Applications of miRNA Technology for Atherosclerosis

Toba, Hiroe; Cortez, Dolores; Lindsey, Merry L.; Chilton, Robert

doi:10.1007/s11883-013-0386-9

Cited by 30 publications

(24 citation statements)

References 20 publications

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“…Interestingly, miR‐10a contributes to the repression of pro‐inflammatory endothelial phenotypes in atherosusceptible regions in vivo 167. In addition, miR‐100, miR‐127, miR‐145, miR‐133a and miR‐133b are increased in carotid plaques in stroke 169. Functionally, miR‐100 and miR‐127 are associated with vascular inflammation 160.…”

Section: Clinical Value Of Mirnas As New Biomarkers For Angiogenesis‐mentioning

confidence: 99%

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The regulatory role of microRNAs in angiogenesis‐related diseases

Sun

Lei

et al. 2018

J Cellular Molecular Medi

119

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MicroRNAs (miRNAs) are small non‐coding RNAs that regulate gene expression at a post‐transcriptional level via either the degradation or translational repression of a target mRNA. They play an irreplaceable role in angiogenesis by regulating the proliferation, differentiation, apoptosis, migration and tube formation of angiogenesis‐related cells, which are indispensable for multitudinous physiological and pathological processes, especially for the occurrence and development of vascular diseases. Imbalance between the regulation of miRNAs and angiogenesis may cause many diseases such as cancer, cardiovascular disease, aneurysm, Kawasaki disease, aortic dissection, phlebothrombosis and diabetic microvascular complication. Therefore, it is important to explore the essential role of miRNAs in angiogenesis, which might help to uncover new and effective therapeutic strategies for vascular diseases. This review focuses on the interactions between miRNAs and angiogenesis, and miRNA‐based biomarkers in the diagnosis, treatment and prognosis of angiogenesis‐related diseases, providing an update on the understanding of the clinical value of miRNAs in targeting angiogenesis.

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Section: Clinical Value Of Mirnas As New Biomarkers For Angiogenesis‐mentioning

confidence: 99%

“…167 In addition, miR-100, miR-127, miR-145, miR-133a and miR-133b are increased in carotid plaques in stroke. 169 Functionally, miR-100 and miR-127 are associated with vascular inflammation. 160 MiR-133 is enriched in cardiomyocytes and regulates myogenesis, cardiac development and hypertrophy.…”

Section: Strokementioning

confidence: 99%

The regulatory role of microRNAs in angiogenesis‐related diseases

Sun

Lei

et al. 2018

J Cellular Molecular Medi

119

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“…Meanwhile, the deposition of modified lipoproteins in the artery wall increases endothelial permeability and promotes the formation of foam cells and necrotic core along with lipid uptake of macrophages [ 2 ]. It is widely recognized that apoptosis in lesional macrophages, along with their defective function in efferocytosis, promotes plaque necrosis, which leads to plaque instability and thrombosis [ 3 , 4 ]. Understanding the multifactorial process consisting of the interactions of several key components, including lipoproteins, inflammatory cells and vascular cells is extremely crucial [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

Exosomal lncRNA GAS5 regulates the apoptosis of macrophages and vascular endothelial cells in atherosclerosis

et al. 2017

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Atherosclerosis is universally recognized as a chronic lipid-induced inflammation of the vessel wall. Oxidized low density lipoprotein (oxLDL) drives the onset of atherogenesis involving macrophages and endothelial cells (ECs). Our earlier work showed that expression of long noncoding RNA-growth arrest-specific 5 (lncRNA GAS5) was significantly increased in the plaque of atherosclerosis collected from patients and animal models. In this study, we found that knockdown of lncRNA GAS5 reduced the apoptosis of THP-1 cells treated with oxLDL. On the contrary, overexpression of lncRNA GAS5 significantly elevated the apoptosis of THP-1 cells after oxLDL stimulation. The expressions of apoptotic factors including Caspases were changed with lncRNA GAS5 levels. Moreover, lncRNA GAS5 was found in THP-1 derived-exosomes after oxLDL stimulation. Exosomes derived from lncRNA GAS5-overexpressing THP-1 cells enhanced the apoptosis of vascular endothelial cells after taking up these exosomes. However, exosomes shed by lncRNA GAS5 knocked-down THP-1 cells inhibited the apoptosis of endothelial cells. These findings reveal the function of lncRNA GAS5 in atherogenesis which regulates the apoptosis of macrophages and endothelial cells via exosomes and suggest that suppressing the lncRNA GAS5 might be an effective way for the therapy of atherosclerosis.

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“…MiRNAs play essential roles in regulating atherosclerosis [5,35,36]. Among all miRNAs, miR-30 has been shown to regulate carcinogenesis of various cancers [37][38][39][40].…”

Section: Introductionmentioning

confidence: 99%

Endothelial Cell Autophagy in Atherosclerosis is Regulated by miR-30-Mediated Translational Control of ATG6

Zhang

Tian

Wang

et al. 2015

Cell Physiol Biochem

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Background/Aims: Endothelial cell injury and subsequent death play an essential role in the pathogenesis of atherosclerosis. Autophagy of endothelial cells has a protective role against development of atherosclerosis, whereas the molecular regulation of endothelial cell autophagy is unclear. MicroRNA-30 (miR-30) is a known autophagy suppressor in some biological processes, while it is unknown whether this regulatory axis may be similarly involved in the development of atherosclerosis. Here, we aimed to answer these questions in the current study. Methods: We examined the levels of endothelial cell autophagy in ApoE (-/-) mice suppled with high-fat diet (HFD), a mouse model for atherosclerosis (simplified as HFD mice). We analyzed the levels of autophagy-associated protein 6 (ATG6, or Beclin-1) and the levels of miR-30 in the purified CD31+ endothelial cells from mouse aorta. Prediction of the binding between miR-30 and 3'-UTR of ATG6 mRNA was performed by bioinformatics analyses and confirmed by a dual luciferase reporter assay. The effects of miR-30 were further analyzed in an in vitro model using oxidized low-density lipoprotein (ox-LDL)-treated human aortic endothelial cells (HAECs). Results: HFD mice developed atherosclerosis in 12 weeks, while the control ApoE (-/-) mice that had received normal diet (simplified as NOR mice) did not. Compared to NOR mice, HFD mice had significantly lower levels of endothelial cell autophagy, resulting from decreases in ATG6 protein, but not mRNA. The decreases in ATG6 in endothelial cells were due to HFD-induced increases in miR-30, which suppressed the translation of ATG6 mRNA via 3′-UTR binding. These in vivo findings were reproduced in vitro on ox-LDL-treated HAECs. Conclusion: Upregulation of miR-30 by HFD may impair the protective effects of endothelial cell autophagy against development of atherosclerosis through suppressing protein translation of ATG6.

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Applications of miRNA Technology for Atherosclerosis

Cited by 30 publications

References 20 publications

The regulatory role of microRNAs in angiogenesis‐related diseases

The regulatory role of microRNAs in angiogenesis‐related diseases

Exosomal lncRNA GAS5 regulates the apoptosis of macrophages and vascular endothelial cells in atherosclerosis

Endothelial Cell Autophagy in Atherosclerosis is Regulated by miR-30-Mediated Translational Control of ATG6

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